MiR‐23b functions as an oncogenic miRNA by downregulating Mcl‐1S in lung cancer cell line A549. Issue 7 (13th April 2020)

• Record Type: Journal Article
• Authors: Wang, Ling; Hu, Zhiyi; Guo, Qi; Yang, Litao; Pang, Yuling; Wang, Wei
• Is Part Of: Journal of biochemical and molecular toxicology. Volume 34:Issue 7(2020)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2020-04-13
• Subjects: Mcl‐1 -- miR‐23b -- NSCLC; Biochemistry -- Periodicals; Molecular biology -- Periodicals; Toxicology -- Periodicals; 574
• DOI: 10.1002/jbt.22494
• Languages: English
• ISSNs: 1095-6670

Abstract

Abstract: It has been reported that microRNA‐23b (miR‐23b) plays a role in multiple cancers, while its impact on lung cancer has not been comprehensively known. Our study explored the probable impacts of miR‐23b on lung cancer cells. Expression of miR‐23b was assessed by reverse transcription quantitative polymerase chain reaction. After miR‐23b mimic, inhibitor, and their own control were transfected into A549 cells, cell viability, migration, invasion, apoptosis, and epithelial‐mesenchymal transition (EMT) were investigated through different experimental methods. The targeting contact between miR‐23b and myeloid cell leukemia‐1 (Mcl‐1) was investigated applying dual‐luciferase activity assay. In addition, the modulatory impacts of miR‐23b on the splicing variants of Mcl‐1 (Mcl‐1S and Mcl‐1L) were explored. MiR‐23b was highly expressed in lung cancer cells compared with normal lung cells. Increased expression of miR‐23b promoted A549 cell viability, migration, invasion, and EMT. However, miR‐23b silencing produced the opposite results. Mcl‐1 has been proven to be a specialized target of miR‐23b. Compared with the reduction of Mcl‐1S induced by miR‐23b overexpression, Mcl‐1L showed negligible interaction with miR‐23b. Moreover, the antitumor activities of miR‐23b silencing were alleviated by Mcl‐1S silencing. The blockage of Janus kinase/signal transducer and activator of transcription protein (JAK/STAT) and Wnt/β‐catenin induced by miR‐23b silencing was reversed by Mcl‐1S silencing. MiR‐23b might be an up‐and‐coming biomarker of lung cancer. In addition, miR‐23b was involved in the tumor‐promoting effects and the mobilization of JAK/STAT and Wnt/β‐catenin pathways through the reduction of Mcl‐1S.